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Melvyn Quan

on 6 March 2018

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Transcript of Herpesviridae

Equid herpesvirus 1 & 4
Highly contagious disease with several clinical syndromes
Infectious bovine rhinotracheitis
Bovine herpesvirus 1 causes several diseases in cattle, including rhinotracheitis, vaginitis, balanoposthitis, abortion, conjunctivitis, and enteritis

Single, linear dsDNA (125-295 kbp)
70 - 200 proteins
Sensitive to dessication, low pH and detergents
± 200 nm
Productive and latent (carrier) cycle
Stress (relapses)
Used for gene therapy
Wide host range, although natural host range of individual viruses very restricted
Upper respiratory and genital tracts
Life-long latent infections
Alphaherpesvirinae - neurons
Betaherpesvirinae - monocytes
Gammaherpesvirinae - lymphocytes
Felid herpesvirus 1
Alcelaphine herpesvirus 1
An acute, systemic viral disease of cattle in close contact with wildebeest.
Wildebeest calves < 4 months NB in transmission - excrete cell-free virus
Also sheep-associated MCF outside Africa.
It is characterized by severe nasal and ocular mucopurulent discharges, eye lesions, and an extremely high case mortality rate once clinical signs have appeared.
Cell-associated (white blood cells).
Lymphoid hyperplasia and lymphocytic infiltration.
It's for life!
core, capsid, tegument and envelope
Bovine herpes, infectious pustular balanoposthitis/vulvovaginitus, vesicular venereal disease, ‘red nose’, ‘dust pneumonia’
Highly contagious
Latent infection
Reactivation following stressor
Route of transmission – close contact or genital
Virus culture – foetel lung, liver, spleen, kidneys, placental tissue. Transport at 4ºC or -70ºC
ID seropositive animals and eliminate from the herd
Latent infections?
Live – intranasal temperature-sensitive mutants
Killed – no cellular or mucosal immunity, but better than live vaccine at reducing viral excretion from latently infected cattle
Subunit – contains gD, but not gE – DIVA
DISC – disabled infectious single cycle vaccine
Route of transmission – close contact or genital
Local lesions in mucous membranes
Vesicles – pustules – erosions – ulcers - necrosis
Latent state in trigeminal or sacral ganglia
Reactivation – viral shedding at same level as 1º infection, but of shorter duration
Reactivation following stressor
Humoral and cellular immunity
Ab’s NB in preventing infection and recovery from 2’ary infections
Cellular immunity involved in recovery once infection is established
Higher the dose, the more severe the infection
Destruction of epth cells, alter muco-ciliary clearance
Fever, RR, coughing, mucopurulent nasal discharge, drop in milk production, erosions
Often 2’ary infection with Mannheimia haemolytica
Also conjunctivitis, abortion
Genital infections (subtype 2)
Clinical signs
Respiratory infections (subtype 1)
Cows – infectious pustular vulvovaginitis (IPV)
Clinical signs 1 to 3 days after mating with an infected bull
Vesicles, pustules, ulcers in the mucosa
Frequent urination, elevated tail, vaginal discharge
Abortions – at any stage of gestation, most commonly around 5th month of pregnancy

Bulls – infectious pustular balanoposthitis (IPB)
Sometimes swollen prepuce, discharge
Semen may contain virus
Bovine herpesvirus 1
(infectious bovine rhinotracheitis)
Canid herpesvirus 1
(canine neonatal herpesvirus infection)
Equid herpesvirus 1 & 4
(equine rhinotracheitis and abortion)
Felid herpesvirus 1
(feline viral rhinotracheitis)
Human herpesvirus 3
Bovine herpesvirus 2
(pseudolumpy skin disease)
Alcephaline herpesvirus 1 (malignant catarrhal fever)
Gallid herpesvirus 2
(Marek's disease)
Bovine malignant catarrhal fever, snotsiekte
Canid herpesvirus 1
Equine rhinopneumonia, equine abortion virus
Direct contact - aerosol
Indirect contact - personnel, equipment, fomites
Routes of infection - inhalation/ingestion
Inapparent and clinical infections (excrete large quantities 7 - 10 days in saliva and nasal discharge)
Abortion/placenta - contaminate environment
Poor immunity
Carrier state
Stress - reactivation
Antigenic change in virus
Source of infection
Inapparent or clinically affected animals
Latently infected animals
Most commonly late pregnancy
Poor humoral response
Short-lived immunity
Does not prevent virus shedding (significantly reduced)
Some cross protecion between EHV-1 an EHV-4
respiratory disease in young animals
peri-natal mortality in foals
paralysis in adult horses
abortion storms in mares
Latent period
Central role of latency
Clinical signs
Stress, introduction of new animals
Clinical signs
Abortions, neurological disease
Virus isolation
Swabs nasopharynx
Buffy coat of blood
Foetal tissue (lungs) and placenta
Brain, spinal chord
CF test
Serum neutralization
collapsed lung
umbilical chord
oedema and congestion of placenta
petechiae in the lung
necrosis and haemorrhages in kidney
petechiae in intestine
respiratory distress in a newborn
poor prognosis
Infection during late gestation
Weak foal born
Death within 3-4 days
Primary lesions associated with respiratory tract
Lungs are firm and voluminous
Atelectasis, sub-mucosal haemorrhages
Enlarged, oedematous and congested bronchial lymph nodes
Intranuclear inclusions in lung cells
Respiratory disease
Normally mild, or subclinical
Most commonly young horses (weanling - 3 years of age)
Stress, overcrowding
Neurological disease
10% of horses develop neurological signs
Infection in endothelial cells of vasculature
Damage to the microvasculature of the CNS
Disseminated ischemic necrosis of the spinal cord
Prevent outbreak
Limit the spread of outbreak
Segregation of pregnant mares from all other horses on the premises.
Isolation for a period of not <3 weeks of all mares entering the stud farm, including those that are returning after leaving the premises.
Subdivision of pregnant mares into small physically separated groups for the duration of gestation.
Stress reduction by avoiding physiological stress.
Disinfection of areas contaminated by virus from the aborted foetus and placental membranes.
Isolation of affected horses.
Submission of clinical samples to a diagnostic laboratory.
Implementation of hygienic procedures to prevent spread of infection (biosecurity).
Use inactivated vaccine
Vaccinate at two-month intervals starting at the fifth month of gestation
Vaccination only reduces virus shedding
Can still get few abortions
Short-lived immunity, can get repeated infections throughout life
Vaccination of pregnant mares to control abortion
virus may not cross placenta
Clinical features
Clinical signs
Temperature sensitive virus
Replicates in cooler nasal passages
Cell associated - mononuclear phagocyte cells
Lymphoid hyperplasia/necrosis
DIC - thrombocytopaenia
Multifocal haemmorhages - vasculitis
Eurican herpes 205 (Merial)
Subunit vaccine
Given to bitches during heat and 1-2 weeks before whelping
better temperature regulation
better developed immunity
Abortion, stillbirth, infertility
CNS signs
Clinical signs
multifocal haemorrhages in kidney
necrotic lesions in lung and liver
multifocal haemmorhages
Vaginitis with vesicular lesion
CaHV-1 IFA nasal turbinates
ulcerative keratitis
nasal and ocular discharge
multifocal lymphoid infiltration in the renal cortex
focally disseminated ulcerative abomasitis
ocular discharge
mucopurulent nasal discharge
exudate in nasopharynx
ulcers on gum
ulcers and erosions
ulcerative interdigital dermatitis
perivascular lymphocytic infiltration
necrotizing vasculitis
oedematous gall-bladder
Disabled infectious single-cycle (DISC) vaccine involve the deletion of an open reading frame coding for a key protein involved in the viral replication or viral capsid formation (Widman et al., 2008). The DISC virus is isolated in cells expressing the key protein, thus providing the missing protein in trans. Such virus, when injected in animals, can complete only one round of replication without producing a progeny virus. Vaccines based on DISC viruses are more stimulatory than a killed virus vaccine and are devoid of problems associated with live vaccines (OIE).
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